Genetic Reassortment of Avian, Swine, and Human Influenza A Viruses in American Pigs

Zhou, Nan; Senne, Dennis A.; Landgraf, John S.; Swenson, Sabrina L.; Erickson, G. A.; Rossow, Kurt; Liu, Lin; Yoon, Karina J.; Krauss, Scott; Webster, Robert G.

doi:10.1128/jvi.73.10.8851-8856.1999

Cited by 510 publications

(248 citation statements)

References 38 publications

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“…Our analysis of this question, completed at the time of publication of the Rest and Mindell paper, differs from their work in the choice of methods, the extent of the genome analyzed, taxon sampling, and in the analysis of nucleotides rather than amino acids. Our results act to both corroborate and extend their findings, adding further support to the idea that SARS has had a recombinant history involving different coronavirus lineages and suggest the possibility that the genome could have arisen through a combination of host jumping and recombination events in a manner analogous to previous outbreaks of influenzae (Gregory et al, 2003;Zhou et al, 1999).…”

Section: Introductionsupporting

confidence: 86%

“…Mixed animal husbandry practices, in proximity to human populations, could have led to the evolution of the SARS coronavirus and facilitated its progression as an infectious disease in humans. Novel human influenza viruses are thought to have arisen from the reassortment, within porcine hosts, of avian, swine, and human influenza viruses (Gregory et al, 2003;Zhou et al, 1999). We suggest that our recombination results for SARS-CoV implicate a suspiciously analogous history.…”

Section: Resultsmentioning

confidence: 74%

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Evidence from the evolutionary analysis of nucleotide sequences for a recombinant history of SARS-CoV

Stanhope

Brown

Amrine-Madsen

2004

Infection, Genetics and Evolution

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The origins and evolutionary history of the Severe Acute Respiratory Syndrome (SARS) coronavirus (SARS-CoV) remain an issue of uncertainty and debate. Based on evolutionary analyses of coronavirus DNA sequences, encompassing an approximately 13kb stretch of the SARS-TOR2 genome, we provide evidence that SARS-CoV has a recombinant history with lineages of types I and III coronavirus. We identified a minimum of five recombinant regions ranging from 83 to 863bp in length and including the polymerase, nsp9, nsp10, and nsp14. Our results are consistent with a hypothesis of viral host jumping events, concomitant with the reassortment of bird and mammalian coronaviruses, a scenario analogous to earlier outbreaks of influenzae.

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Section: Introductionsupporting

confidence: 86%

Section: Resultsmentioning

confidence: 74%

Evidence from the evolutionary analysis of nucleotide sequences for a recombinant history of SARS-CoV

Stanhope

Brown

Amrine-Madsen

2004

Infection, Genetics and Evolution

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“…Coinfection of a single cell with multiple viral strains allows genetic recombination, a major event driving viral diversity and escape from available antiviral drugs and vaccine-induced immunity (368)(369)(370). With segmented viruses, reassortment of the viral segments is a major source for the generation of novel viruses (371)(372)(373). The major influenza A pandemics in 1957, 1968, and 2009 all emerged from reassortment of viral segments (374).…”

Section: Genetic Recombination and Virus Evolutionmentioning

confidence: 99%

Virological and Immunological Outcomes of Coinfections

et al. 2018

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SUMMARYCoinfections involving viruses are being recognized to influence the disease pattern that occurs relative to that with single infection. Classically, we usually think of a clinical syndrome as the consequence of infection by a single virus that is isolated from clinical specimens. However, this biased laboratory approach omits detection of additional agents that could be contributing to the clinical outcome, including novel agents not usually considered pathogens. The presence of an additional agent may also interfere with the targeted isolation of a known virus. Viral interference, a phenomenon where one virus competitively suppresses replication of other coinfecting viruses, is the most common outcome of viral coinfections. In addition, coinfections can modulate virus virulence and cell death, thereby altering disease severity and epidemiology. Immunity to primary virus infection can also modulate immune responses to subsequent secondary infections. In this review, various virological mechanisms that determine viral persistence/exclusion during coinfections are discussed, and insights into the isolation/detection of multiple viruses are provided. We also discuss features of heterologous infections that impact the pattern of immune responsiveness that develops.

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“…However, the majority of the SIV infections in pigs are caused by subtypes H1N1, H1N2 and H3N2 [1]. Emergence of the H3N2 subtype containing a triple reassortment internal gene (TRIG) cassette contributed vastly to the generation of antigenic divergent reassortant viruses [2,3]. The hemagglutinin (HA) gene in these H3N2 viruses was derived from the different seasonal human influenza viruses.…”

Section: Introductionmentioning

confidence: 99%

Poly I:C adjuvanted inactivated swine influenza vaccine induces heterologous protective immunity in pigs

Thomas

Wang

Sreenivasan

et al. 2015

Vaccine

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Swine influenza is widely prevalent in swine herds in North America and Europe causing enormous economic losses and a public health threat. Pigs can be infected by both avian and mammalian influenza viruses and are sources of generation of reassortant influenza viruses capable of causing pandemics in humans. Current commercial vaccines provide satisfactory immunity against homologous viruses; however, protection against heterologous viruses is not adequate. In this study, we evaluated the protective efficacy of an intranasal Poly I:C adjuvanted UV inactivated bivalent swine influenza vaccine consisting of Swine/OH/24366/07 H1N1 and Swine/CO/99 H3N2, referred as PAV, in maternal antibody positive pigs against an antigenic variant and a heterologous swine influenza virus challenge. Groups of three-week-old commercial-grade pigs were immunized intranasally with PAV or a commercial vaccine (CV) twice at 2 weeks intervals. Three weeks after the second immunization, pigs were challenged with the antigenic variant Swine/MN/08 H1N1 (MN08) and the heterologous Swine/NC/10 H1N2 (NC10) influenza virus. Antibodies in serum and respiratory tract, lung lesions, virus shedding in nasal secretions and virus load in lungs were assessed. Intranasal administration of PAV induced challenge viruses specific-hemagglutination inhibition- and IgG antibodies in the serum and IgA and IgG antibodies in the respiratory tract. Importantly, intranasal administration of PAV provided protection against the antigenic variant MN08 and the heterologous NC10 swine influenza viruses as evidenced by significant reductions in lung virus load, gross lung lesions and significantly reduced shedding of challenge viruses in nasal secretions. These results indicate that Poly I:C or its homologues may be effective as vaccine adjuvants capable of generating cross-protective immunity against antigenic variants/heterologous swine influenza viruses in pigs.

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Genetic Reassortment of Avian, Swine, and Human Influenza A Viruses in American Pigs

Cited by 510 publications

References 38 publications

Evidence from the evolutionary analysis of nucleotide sequences for a recombinant history of SARS-CoV

Evidence from the evolutionary analysis of nucleotide sequences for a recombinant history of SARS-CoV

Virological and Immunological Outcomes of Coinfections

Poly I:C adjuvanted inactivated swine influenza vaccine induces heterologous protective immunity in pigs

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